Project description:To identify mRNA substrates for the human RNase MRP complex, we examined the effects of siRNA-mediated depletion of RNase MRP (and RNase P) on the transcriptome of HEp-2 cells. The expression of two RNase MRP protein components, hPop1 and Rpp40, was knocked-down and after 48 hours mRNA was isolated from these cells as well as from cells transfected with an siRNA targeting the GFP mRNA (siEGFP), which was used as a control. The expression levels of mRNAs were analyzed on a genome-wide scale using 21K microarrays.
Project description:analysis of differential gene expression in CD34+ derived neutrophil progenitors from umbilical cord blood, in response to Mek1 activation
Project description:Tissue specific microarray data is obtained by generating a whole-organism extract and subsequent co-immune precipitation of mRNA with the poly-A binding protein FLAG::PAB-1 specifically expressed in body wall muscle cells (Roy et al. 2002). Different lines were compared: SV911 (control), SV912 (CYE-1/CDK-2AF), and SV985 (CYD-1/CDK-4). As reference total RNA was used.
Project description:This experiment evaluates quick (alarm) response to chilling in chilling-sensitive maize plants.<br>Maize inbred line cm109 were grown in optimal conditions until third leaf was fully developed. <br>At this stage plants were divided into three experimental variants: k0 - control plants, frozen<br>at the beginning of daylight, k4 - control plants kept in the same conditions and frozen after 4 hours<br>since beginning of daylight, c4 - plants kept in 14 deg. C for 4 hours since "dawn". At the mentioned<br>moments, leaves were harvested and frozen in liquid nitrogen for RNA isolation.
Project description:Gene expression in the fetal liver cells obtained from MBT-1+/+ or MBT-1-/- embryos at E14.5 were analyzed using Affymetrix Genechip to assess the effect of the gene knock-out on hematopoietic cells.
Project description:A comparison of Ostes homozygous mutant soleus muscles to wildtype soleus muscles. Hybridisation of 3 Mouse CNG 25k oligo arrays, using 3 pools of 10 mice(5 male and 5 female) for mutant and WT.<br><br>
Project description:Transformants either containing pCS1 (strain CCS1) or pNIM as control (strain CCS2) were induced by doxycycline (40 ï¾µg/ml) for the indicated times (T0-T10, 0 to 10 min) in hypha-inducing medium (10 % serum, 37 ï¾°C) under a stream of 93.8 % nitrogen, 6 % CO2 and 0.2 % oxygen. For each time point, cDNA of CCS1 and CCS2 were co-hybridised to microarrays and ratios of expression were calculated for each gene. Each gene is represented by duplicate spots on the DNA microarrays.
Project description:Transformants either containing pCS1 (strain CCS1) or pNIM as control (strain CCS2) were induced by doxycycline (40 ï¾µg/ml) for the indicated times (T0-T10, 0 to 10 min) in aerated hypha-inducing medium (10 % serum, 37 ï¾°C). For each time point, cDNA of CCS1 and CCS2 were co-hybridised to microarrays and ratios of expression were calculated for each gene. Each gene is represented by duplicate spots on the DNA microarrays.
Project description:<br><br>Annual heart allograft failure in humans rates about 3-5%. The main reason after the first postoperative year is chronic rejection. Myointimal hyperplasia, the hellmark of chronic rejection, results in a specific type of ischemic heart disease. The lack of angina pectoris symptoms allow ventricular arrythmias, sudden cardiac death or heart failure to occur without warning. In addition, diagnostic tools such as endomyocardial biopsy, coronary angiography or intracoronary ultrasound fail to predict the individual risk for myocardial dysfunction.<br><br>The mechanisms responsible for chronic rejection are predominantly alloimmune mediated with activated T cells, macrophages, B cell mediated antibody formation and secreted cytokines responding to HLA and other endothelial cell antigens. In addition, non immunologic risk factors such as recipient age, metabolic factors, hypertension and ischemia contribute to development of this disease. Previous studies have demonstrated that ischemia has a profound influence on short term allograft survival but the underlaying mechanisms remain largely unknown. Apoptosis seems to play a crucial role in ischemia/reperfusion injury and several mechanisms for programmed cell death have been described. However, consequences on long term cell function of viability have not been investigated. <br><br>The aim of this study was to investigate the implication and the mechanism of prolonged cold organ storage as a non immunologic risk factor in the pathogenesis of chronic rejection in a cardiac allograft model. <br><br>We aimed for answering the following specific questions:<br><br>How does cold ischemia affect the alloimmue response short and long term? <br><br>How does prolonged cold ischemia affect gene expression at later time points after transplantation? <br><br>Does it influence gene expression during chronic rejection?<br><br><br><br>